
The '20s may have been roaring for well-heeled urban centers, but on the farm? Rural electricity in the 1920s was as rare as Google Fiber is today. Which makes these 1922 predictions for the farm of the future so brazen.
Climate change causing greenhouse gases, particularly carbon dioxide (CO2), will cause less rain in areas that need it most and more rain in areas that need it least. According to recent NASA findings areas that get a lot of rain will get more, those areas that get moderate rainfall will get less, and those areas that get little rainfall may get none at all.
NASA?s research is the product of an analysis of the computer simulations from 14 climate models. They span 140 years and they show that warming from carbon dioxide will change the frequency that regions around the planet receive rain.
Some parts of the world will see significant increases in rainfall. These areas include tropical zones around the equator, particularly in the Pacific Ocean and Asian monsoon regions.
While some parts of the world will suffer from too much rain, other parts of the world will suffer from extreme drought. By 2050 NASA?s research indicates that there will be no rain in much of the Southwest and California. The Amazon are also expected to suffer from ?megadroughts.?As explained in a NASA news release:
?Some regions outside the tropics may have no rainfall at all. The models also projected for every degree Fahrenheit of warming, the length of periods with no rain will increase globally by 2.6 percent. In the Northern Hemisphere, areas most likely to be affected include the deserts and arid regions of the southwest United States, Mexico, North Africa, the Middle East, Pakistan, and northwestern China. In the Southern Hemisphere, drought becomes more likely in South Africa, northwestern Australia, coastal Central America and northeastern Brazil.?
Some of the most devastating impacts of reduced rainfall will be felt in areas that get moderate rainfall because this is where most people live. Water is essential for life and rainfall is also a critical element of food production. These new precipitation patterns will lead to increased water scarcity and food shortages. It is likely that this will cause major climate change related migrations.
NASA?s latest research findings are not spurious, they are corroborated a slew of other studies which have come to the same conclusions.
? 2013, Richard Matthews. All rights reserved.Source: http://www.greenconduct.com/news/2013/06/02/co2-will-adversely-impact-rainfall-around-the-world/
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Source: http://glona38.blogspot.com/2013/06/pure-adrenaline-boston-action-sports.html
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NEW YORK (Reuters) - Manufacturing picked up slightly in May, a survey showed on Monday, though the pace was still sluggish and suggested the sector may be a drag on the economy in the second quarter.
Financial data firm Markit said its final Manufacturing Purchasing Managers Index (PMI) rose to 52.3 in May from 52.1 in April, which was better than the preliminary reading of 51.9.
A reading above 50 indicates expansion.
Growth in output eased for the third straight month, with the sub-index slipping to 52.7 from 53.7, while the pace of hiring in the sector fell to a six-month low.
"The survey paints a downbeat picture of manufacturing business conditions. Output, order books and employment are all growing modestly, suggesting the sector is at risk of stalling," said Chris Williamson, Markit chief economist.
The gauge of new orders from domestic clients rose to 53.3 from 51.5, helping the main index improve slightly on April's result. That also helped make up for a decline in overseas orders, which fell for the first time in three months.
Williamson said slower growth in the factory sector was likely to contribute to weaker economic growth in the second quarter.
The economy expanded at a 2.4 percent pace between January and March, a hefty jump over 0.4 percent in the final three months of 2012.
But economists suspect a manufacturing slowdown and a drop in government spending could sap it of momentum in the second quarter, repeating a pattern seen over the past two years.
The Institute for Supply Management's manufacturing purchasing managers index for April showed the sector's growth slowed. The May report, due later on Monday, was expected to show the sector remained sluggish.
Consumer spending also fell in April for the first time in nearly a year and price pressures were subdued, suggesting the Federal Reserve may have to maintain its monetary stimulus for a while yet.
The Markit index found that goods-producing firms reported higher input prices in May, though the rate of increase remained much weaker than that seen at the start of the year. Output charges rose modestly on the month.
(Reporting By Steven C. Johnson; Editing by Chizu Nomiyama)
Source: http://news.yahoo.com/factory-activity-edges-may-growth-sluggish-markit-130055806.html
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Authorities in Vallejo, Calif. say that Anthony Cardenas painted this crosswalk at a busy intersection himself.
VALLEJO, Calif. -- A Northern California man is facing vandalism charges after authorities say he painted a crosswalk on a street, allegedly telling officials it was needed.
Fifty-two-year-old Anthony Cardenas was arrested Thursday morning in Vallejo and booked into Solano County Jail on suspicion of felony vandalism. Solano County Sheriff's Lt. Brad DeWall says workers spotted Cardenas committing the vandalism at a city intersection.
The intersection already has three crosswalks.
DeWall says Cardenas also painted lines through those.
State transportation workers painted over Cardenas' alleged crosswalk later in the day. A police cadet had been posted at the intersection until then to keep pedestrians from using it.
Cardenas remained behind bars Friday on $15,000 bail. Dewall says he did not have an attorney.
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June 1, 2013 ? Spouses and long-term partners of patients with mouth and throat cancers related to infection with the human papilloma virus (HPV) appear to have no increased prevalence of oral HPV infections, according to results of a multicenter, pilot study led by Johns Hopkins investigators. The study?s results suggest that long-term couples need not change their sexual practices, say the scientists.
?While we can?t guarantee that the partners of patients will not develop oral HPV infections or cancers, we can reassure them that our study found they had no increased prevalence of oral infections, which suggests their risk of HPV-related oral cancer remains low,? says Gypsyamber D?Souza, Ph.D., M.P.H., associate professor of epidemiology at the Johns Hopkins University Bloomberg School of Public Health. She is expected to present the results of her study June 1 at the 2013 American Society of Clinical Oncology Annual Meeting.
HPV-related oral cancers are rising in prevalence among white men in the United States, and fear of transmitting the virus can lead to anxiety, divorce, and curtailing of sex and intimacy among couples, says D?Souza. Persistent oral HPV infections are a risk for developing oropharyngeal cancers, located at the base of the tongue, tonsils, pharynx and soft palate.
At the Johns Hopkins Hospital and three other hospitals, researchers conducted surveys and took oral rinse samples from 166 male and female patients with HPV-related oropharyngeal cancers and 94 spouses and partners. The scientists also studied patients? tumor samples and performed visual oral examinations of spouses/partners. Of the 94 spouses/partners, six were male.
More than half of patients had at least one type of HPV DNA detectable in their oral rinses, including HPV16, the viral type most commonly associated with oral and other cancers. After a year, only seven patients (six percent) still had oral HPV16 DNA detectable.
Of the 94 spouses/partners, six had oral HPV infections (6.5 percent). Among the six, none of the men and two of four females (2.3 percent) had HPV16 infections at very low levels. These infections were not detectable one year later. No oral cancers were detected among 60 spouses/partners who underwent a visual oral exam.
One spouse and one patient reported a history of cervical cancer. Two spouses reported a history of cervical pre-cancer, and three patients said they had previous spouses with cervical cancers, but these were self-reported, unconfirmed cases.
?The oral HPV prevalence among partners who participated in this study are comparable to rates observed among the general population,? says D?Souza. ?We suspect that long-term spouses and partners have been exposed to HPV, like most of us, and appear to have cleared the virus.?
D?Souza and her colleagues recommend that long-term couples need not change their sexual practices. ?Certainly, with new sexual partners, caution is always advised.?
More research is needed to determine the timeline of progression for HPV-related oral cancers and how HPV is transmitted and suppressed by the immune system, adds D?Souza.
Funding for the study was provided by the Johns Hopkins Innovation Fund and the Richard Gelb Cancer Prevention Award.
Scientists contributing to the research include Neil Gross from the Oregon Health & Science University; Maura Gillison from the Ohio State University; Sara Pai from Johns Hopkins; Robert Haddad from the Dana Farber Cancer Center; and Marshall Posner from Mount Sinai Medical Center.
ASCO Abstract #6031: Oral HPV infection in HPV-positive oropharyngeal cancer cases and their spouses.
Source: http://feeds.sciencedaily.com/~r/sciencedaily/health_medicine/genes/~3/ViWwN0OExCc/130601133643.htm
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CHARLOTTESVILLE, Va. (AP) ? Corey Dick homered and had three of UNC Wilmington's 16 hits, and the Seahawks eliminated mistake-prone Army from the NCAA tournament Saturday with a 9-5 victory that ended on a bizarre triple play.
With Army trailing by four and no outs, Jon Crucitti struck out with two runners on ? and both running on the pitch. Lead runner Michael Sands was caught between second and third, and retreated to second, where Grant Van Orden was already standing. Third baseman Ryan LaGrange tagged Van Orden out, and Sands inexplicably broke for third, where LaGrange threw to catcher Drew Farber for the final out.
The Seahawks (38-22), who scored nine runs in the first four innings, got two RBIs each from Tyler Molinaro and Matt Keeler.
Army (29-23) had just seven hits. A three-run sixth pulled the Black Knights within 9-5, but they left the bases loaded in the eighth.
Source: http://news.yahoo.com/unc-wilmington-eliminates-army-triple-play-213246138.html
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The Cook Political Report has announced it's shifting its prediction for the Massachusetts Senate race from 'leaning Democrat' to 'toss up.' In 2010, Republican Scott Brown won a similar special election.
By Ryan Lenora Brown,?Correspondent / May 31, 2013
This combination of photos shows Democrat Rep. Ed Markey (l.) and Republican Gabriel Gomez, candidates for US Senate in the June special election, being held to fill John Kerry's former Senate seat.
AP
EnlargeSpecial elections are a fickle breed.?
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Their turnout is low, the partisanship of voters is high, and those running have to campaign without the energy boost of other candidates vying for office all around them.
In Massachusetts this June, that volatility could make for a tighter-than-expected contest in the race for John Kerry?s former Senate seat, according to a new analysis by the nonpartisan Cook Political Report.
The Cook report announced Thursday that it was shifting its prediction for the race from ?leaning Democrat? to ?toss up,? although the group acknowledged it still had its ?thumb on the scale? for Democrat Edward Markey, an 18-term congressman who has consistently polled ahead of his Republican rival, businessman Gabriel Gomez.?
?In truth, we have had a difficult time accepting the idea that this race might get close,? wrote Cook?s Jennifer Duffy. ?At the same time, Democrats nominated a long-serving member of Congress at a time when Congress is an almost universally unpopular institution. It doesn?t help that Markey has not had a competitive race in decades.?
As the report notes, there?s still a lot going against Mr. Gomez in this race, right down to the basics: He?s a Republican paddling through a deep sea of blue. Registered Democrats outflank their GOP counterparts in Massachusetts by a margin of 3 to 1.
He also has less money, less clout, and less of an organizing base to kick-start get-out-the-vote efforts than does Mr. Markey, who brought first lady Michelle Obama to Boston earlier this week for a swanky lunch that raised more than $700,000 for his campaign.
Cajoling would-be voters to the polls will be key in this race, says Marc Landy, a political scientist at Boston College, because in a special election, ?it?s all about turnout.?
Specifically, more than half of Massachusetts voters are registered as independents, and Gomez will need to get as many of them as possible to the polls June 25.?
Recent history suggests that?s possible. In 2010, Republican Scott Brown won a similar special election on the strength of his support from independents, who voted for him 2 to 1 over Democratic Martha Coakley, according to a postelection poll by The Washington Post.
In a Public Policy Polling survey released in mid-May, Gomez had 56 percent of the independent vote ? up from 47 percent at the beginning of the month.
But polls for special elections are notoriously hard to read, the Cook analysis points out, since it?s hard for pollsters to accurately predict who will vote. That?s led to a wild range of margins in this campaign so far, with polls showing Markey leading by anything from three to 17 points.
Although Markey remains solidly ahead, this election is about more than who wins next month, Mr. Landy says.
?If Gomez were even to come close to Markey, that would indicate some real displeasure with the [Obama] administration in Massachusetts,? he says.
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OKLAHOMA CITY (AP) ? National Weather Service meteorologists say it's unclear how many tornadoes touched down Friday evening.
Dozens of tornado warnings were issued across a wide swath of the Midwest, including Oklahoma and Missouri, as a large storm front moved through the region. Nine died and dozens were injured.
Weather service meteorologists said Saturday that crews have to assess the damage before determining whether it was caused by tornadoes or severe thunderstorms. Cars were toppled on an interstate in the Oklahoma City area, and aerial images showed damaged to homes and businesses in the suburbs of St. Louis.
They said they expected to have an estimate by Saturday afternoon.
A cold front will move through the Plains and Midwest today, lessening the chances for severe weather.
Source: http://news.yahoo.com/nws-number-midwest-plains-tornadoes-unclear-133458553.html
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OAKLAND, Calif. (AP) ? All-Star forward David Lee made a surprising return for the Golden State Warriors in Game 6 against the Denver Nuggets on Thursday night after not dressing the previous four games with what the team had called a season-ending hip injury.
Lee didn't participate in early pregame warm-ups, then sprinted out of the tunnel second behind Stephen Curry about 15 minutes before tipoff, ripping off his jacket and getting a rousing ovation from fans when he was shown on the videoboard.
With 6:05 remaining in the first quarter, Lee took off the shirt over his uniform and began to check in at the scorer's table. As fans started to roar to its feet, Nuggets coach George Karl quickly called timeout and quieted the crowd.
Lee didn't come in following the timeout, then went back to the scorer's table once played resumed. He finally entered the game with 2:23 to play following a timeout by Warriors coach Mark Jackson, getting a standing ovation from fans as he jogged to center court and pointed to the sky with both hands.
Lee had one rebound and missed his only shot in 87 seconds of play in the first quarter.
Lee was hurt in the fourth quarter of Game 1, when he banged into Denver's JaVale McGee on a drive and landed on his side. The Warriors said April 21 he had a season-ending tear of his right hip flexor.
Carl Landry started at power forward alongside point guard Stephen Curry, shooting guard Klay Thompson, small forward Harrison Barnes and center Andrew Bogut.
Lee gave Jackson a hug and the two spoke for a few seconds while the lights dimmed during player introductions. Lee led the pep talk in the huddle after starters were announced.
Source: http://news.yahoo.com/david-lee-returns-warriors-game-6-vs-denver-042343435.html
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The Hill:
The Republican establishment breathed a sigh of relief when Boston businessman Gabriel Gomez won Tuesday's GOP primary in the Massachusetts special Senate race, believing he represents the party's best chance at an unlikely pick-up in liberal Massachusetts.
Read the whole story at The Hill
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In a study using mice, researchers from the University of North Carolina at Chapel Hill found that a hormone, adrenomedullin, plays a crucial role in preventing the pregnancy complication preeclampsia. Surprisingly, this hormone protects women from preeclampsia when emitted by the fetus, not the mother, during the most critical times in pregnancy.
"We've identified the fact that the baby is important in protecting the mom from preeclampsia," said the study's senior author, Kathleen M. Caron, Ph.D., Assistant Dean for Research at the UNC School of Medicine and an associate professor in the Department of Cell Biology and Physiology. "If the baby's cells are not secreting this hormone, the mother's blood vessels don't undergo the dilation that they should."
Preeclampsia affects roughly one in fifteen pregnancies. An important characteristic of the condition is that blood vessels in the placenta fail to enlarge, or dilate, to accommodate increased blood flow to the fetus. Untreated, it can threaten the life of both mother and baby.
"We really don't know that a pregnant woman is going to get preeclampsia until she has it," said Caron. Because the condition has numerous risk factors and causes, it's difficult for doctors to know which patients are at highest risk. "Identifying molecules that could predict preeclampsia would be really important."
The researchers studied mice that were genetically programmed to produce either reduced or increased levels of adrenomedullin. The study revealed that in a normal pregnancy, the fetus secretes adrenomedullin into the placenta during the second trimester, signaling special cells called "natural killer cells" to help dilate the mother's blood vessels and allow more blood to flow to the growing fetus.
The study is one of the first to identify an important chemical message sent from fetus to mother in the womb. Scientists understand more about the mom's side of the 'chemical conversation' that goes on between mother and baby, but much of the hormonal signaling in the placenta remains a mystery.
By identifying the key role of adrenomedullin, the research could pave the way to new methods for detecting and preventing preeclampsia. For example, adrenomedullin levels could potentially be used as a biomarker, or early indicator, to identify which patients might be predisposed to the condition. "Having a biomarker would be wonderful?it could allow the physician to manage a woman differently in the early part of her pregnancy," said Caron.
As a next step, the researchers plan to build upon their mouse studies to examine patterns of adrenomedullin levels and preeclampsia in pregnant women.
###
This paper was published online ahead of print on May 1, 2013 in the Journal of Clinical Investigation (JCI). The paper will appear in the June 2013 print edition.
University of North Carolina Health Care: http://www.med.unc.edu
Thanks to University of North Carolina Health Care for this article.
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There's are kinds of asteroids and other debris cruising through space, but a lot of the really dangerous stuff is stuff we put there ourselves. NASA's cosmic bubble-spotting Fermi telescope
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BARCELONA, Spain (AP) ? The Champions League final will feature two German teams for the first time after Bayern Munich completed surprising 7-0 rout of Barcelona.
Playing with a big cushion after a 4-0 win in the first leg at home last week, Bayern beat Barcelona 3-0 in the second leg Wednesday night on goals by Arjen Robben in the 48th minute and Thomas Mueller in the 76th around Gerard Pique's own goal in the 72nd.
Bayern, which relaxed when it saw injured Lionel Messi wasn't in Barcelona's starting lineup, is in the final for the third time in four years and will play Borussia Dortmund at London's Wembley Stadium on May 25.
"I think it is a terrific performance, it is a little bit of history," Robben said. "If we perform like this, against a team who have dominated Europe for the past five years, who have so much quality, it is amazing."
This final wll be just the fourth single-nation championship match in Europe. Real Madrid beat Valencia in 2000, AC Milan defeated Juventus in 2003 and Manchester United edged Chelsea in 2008.
Bayern will be seeking its fifth title, and first since 2001, while Dortmund won its only championship in 1997. Bayern, which clinched the Bundesliga title on April 6 with six games to spare, travels to Dortmund for a league match Saturday night.
"I'm sure we'll celebrate with a few beers tonight," Bayern captain Philipp Lahm said. "I've always said we have special characters in our squad, and that we are capable of great things."
Bayern lost last year's final at home to Chelsea on penalty kicks, two years after it was defeated 2-0 by Inter Milan.
While many expected Barcelona to meet Real Madrid in the final, Dortmund defeated Madrid 4-1 in Germany last week and hung on Tuesday for a 4-3 aggregate win.
Bayern had no such scare. Missing Messi, the four-time world player of the year who has hampered by a hamstring injury for the past month, Barcelona showed little offensive spark.
"When we saw his name wasn't in the starting lineup, we breathed a sigh of relief," Bayern midfielder Javi Martinez said.
Messi started in the first leg but was largely ineffective, and didn't get off the substitutes bench for the second.
"We trained today but he wasn't comfortable, and we decided that if we were going to risk him it would be at the end," Barcelona coach Tito Vilanova said.
Bayern made sure the final minutes didn't mattter.
"I do not think his participation tonight would have changed things all that much," Pique said. "It isn't pleasant living through a situation like this. In the first half we really tried but when they scored the first, we were left feeling down. We have to congratulate Bayern, who were superior."
When Xavi Hernandez and Andres Iniesta were substituted in the second half, it left Barcelona without its three biggest stars on the field. Barcelona also was missing defenders Carles Puyol and Javier Mascherano and midfielder Sergio Busquets because of injuries, and left back Jordi Alba because of a suspension for yellow-card accumulation.
While Barcelona has an 11-point lead in the Spanish league with five games left, its first season since Vilanova replaced Pep Guardiola as coach will be considered a disappointment because it failed to win the Champions League following titles in 2006, 2009 and 2011.
Guardiola was hired by Bayern in January to replace Jupp Heynckes as coach at the end of the season.
"When the draw came out and we were paired with Barcelona, I would never have imagined that we would win 4-0 and then 3-0 at the Camp Nou," Heynckes said "Barcelona is a fantastic team. Today it had personnel problems, when Messi plays it is very different."
NOTES: Barcelona had gone unbeaten in 21 Champions League home matches since its 2-1 loss to Rubin Kazan on Oct. 20, 2009. ... Barcelona goalkeeper Victor Valdes became the 17th player to make 100 Champions League appearances.
Source: http://news.yahoo.com/bayern-munich-dortmund-german-champs-final-204213422.html
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Contact: Caroline Arbanas
arbanasc@wustl.edu
314-286-0109
Washington University School of Medicine
The most in-depth look yet at endometrial cancer shows that adding genomics-based testing to the standard diagnostic workup could change the recommended course of treatment for some women.
The new research, involving nearly 400 women with endometrial cancer, is published May 2 in the journal Nature. The endeavor is part of The Cancer Genome Atlas project, funded by the National Institutes of Health (NIH).
The study also indicates that some endometrial tumors are genetically similar to subtypes of ovarian cancer and deadly basal-like breast cancer. Future clinical trials should evaluate whether some endometrial cancers could be treated with drugs typically used for the other cancers, says project co-leader Elaine Mardis, PhD, co-director of The Genome Institute at Washington University School of Medicine in St. Louis. The other co-leader is Douglas A. Levine, MD, of the Memorial Sloan-Kettering Cancer Center.
A second Cancer Genome Atlas paper will be published May 1 in the New England Journal of Medicine. That research, also led by Washington University, describes finding virtually all the major mutations involved in acute myeloid leukemia.
While gynecologic oncologists have long recognized two subtypes of endometrial cancer, one more aggressive than the other, the new data reveal four novel subtypes and also suggest that the frequency of mutations in a tumor could be used to help guide treatment decisions.
"We are entering an era when tumors can be evaluated from a genomics standpoint, not just by looking at cancer cells under a microscope," Mardis says. "This more comprehensive approach provides a clearer picture of the way particular endometrial cancers will behave and will be important to gynecological oncologists who treat this disease."
As part of the new research, a consortium of researchers analyzed tumors from 373 women with endometrial cancer using different technologies to look for defects in DNA, RNA (a close chemical cousin of DNA) and proteins.
Their analysis indicates that about 25 percent of women with endometrial cancer who are thought to have a favorable prognosis based on pathology reports instead have a more formidable form of the disease, based on underlying genetic changes, and should be treated aggressively.
Clinically, endometrial cancers fall into two categories: endometrioid and serous. Endometrioid cancers generally are associated with excess estrogen, obesity and a favorable prognosis. In contrast, serous endometrial cancers are more common in older women and generally have poorer outcomes.
After surgery to remove endometrial cancer, women with the endometrioid subtype typically are treated with radiation therapy to kill remaining cancer cells, while those with serous tumors receive a more aggressive treatment chemotherapy.
Doctors distinguish between the two tumor subtypes by evaluating cancer cells under a microscope. But categorizing some tumors is difficult, and pathologists don't always agree.
Looking closely at endometrioid tumors classified as high-grade, meaning they are more likely to grow quickly and spread, the investigators showed that many share genetic features with serous tumors. These include frequent mutations in TP53, a tumor suppressor gene, as well as extensive copy number alterations, which refer to a cell having too many or too few copies of a gene.
"This highlights the benefit of digging deeper to find the genetic drivers of cancer growth," Mardis says. "Even though high-grade endometrioid and serous endometrial cancer are different from a pathological standpoint, they are genetically very similar and may require a similar course of treatment."
With a complete analysis of the tumor samples, the investigators identified four novel genomic-based subtypes of endometrial cancer, which set the stage for developing new ways to diagnose and treat the disease. The subtypes are based, in part, on the frequency of mutations in the tumors.
"The Cancer Genome Atlas' multidimensional approach to collecting genomic data, including clinical and pathology information, have made these findings possible," says Harold Varmus, MD, director on the National Cancer Institute. "Without the integrated characterization of so many tumor samples, correlations between histology and genomic data may not have been observed or potential clinical outcomes identified."
Interestingly, one subtype features an exceedingly high mutation rate in the POLE gene and, in this respect, is similar to an "ultramutated" subtype of colorectal cancer. But, surprisingly, patients with these kinds of tumors generally have good outcomes.
"Having many, many mutations sounds like a bad thing," Mardis explains. "But these patients can't fix the mistakes in their tumor DNA, so their cancer cells mutate themselves into oblivion before they have the opportunity to spread to other locations in the body. The good news for these patients is that their outcomes are excellent, and they don't need aggressive treatment."
Women with serous tumors frequently had mutations in one of two genes that potentially could be targeted with existing targeted therapies. Those with ERBB2 alterations, for example, may be effectively treated with Herceptin, a drug typically used in women with breast cancer who have the same mutation. Additionally, women whose endometrial tumors have PIK3CA mutations may benefit from drugs that inhibit the gene. Those drugs are now in phase II clinical trials.
According to the authors, the new findings provide a roadmap for future clinical trials for endometrial cancer.
"Each tumor subtype may warrant separate clinical trials because of marked genomic differences, which are indicative of different drivers of endometrial cancer," Mardis says. "Developing therapies for each subtype may improve outcomes for many women with endometrial cancer and parallel what has been accomplished in breast cancer."
Endometrial cancer is the fourth most commonly diagnosed cancer among U.S. women. About 50,000 cases will be diagnosed in 2013, and an estimated 8,000 women will die from the disease. For a majority of patients diagnosed with aggressive, high-grade tumors that have spread, the five-year survival rate is about 16 percent, though chemotherapy has been associated with improved survival, and new targeted agents are being tested.
###
Levine DA, Mardis ER and The Cancer Genome Atlas Research Network. Integrated genomic characterization of endometrial carcinoma. Nature. May 2, 2013.
The research is funded by the National Institutes of Health (NIH) as part of The Cancer Genome Atlas Project. Grant numbers: 5U24CA143799-04, 5U24CA143835-04, 5U24CA143840-04, 5U24CA143843-04, 5U24CA143845-04, 5U24CA143848-04, 5U24CA143858-04, 5U24CA143866-04, 5U24CA143867-04, 5U24CA143882-04, 5U24CA143883-04, 5U24CA144025-04, U54HG003067-11, U54HG003079-10 and U54HG003273-10.
Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Contact: Caroline Arbanas
arbanasc@wustl.edu
314-286-0109
Washington University School of Medicine
The most in-depth look yet at endometrial cancer shows that adding genomics-based testing to the standard diagnostic workup could change the recommended course of treatment for some women.
The new research, involving nearly 400 women with endometrial cancer, is published May 2 in the journal Nature. The endeavor is part of The Cancer Genome Atlas project, funded by the National Institutes of Health (NIH).
The study also indicates that some endometrial tumors are genetically similar to subtypes of ovarian cancer and deadly basal-like breast cancer. Future clinical trials should evaluate whether some endometrial cancers could be treated with drugs typically used for the other cancers, says project co-leader Elaine Mardis, PhD, co-director of The Genome Institute at Washington University School of Medicine in St. Louis. The other co-leader is Douglas A. Levine, MD, of the Memorial Sloan-Kettering Cancer Center.
A second Cancer Genome Atlas paper will be published May 1 in the New England Journal of Medicine. That research, also led by Washington University, describes finding virtually all the major mutations involved in acute myeloid leukemia.
While gynecologic oncologists have long recognized two subtypes of endometrial cancer, one more aggressive than the other, the new data reveal four novel subtypes and also suggest that the frequency of mutations in a tumor could be used to help guide treatment decisions.
"We are entering an era when tumors can be evaluated from a genomics standpoint, not just by looking at cancer cells under a microscope," Mardis says. "This more comprehensive approach provides a clearer picture of the way particular endometrial cancers will behave and will be important to gynecological oncologists who treat this disease."
As part of the new research, a consortium of researchers analyzed tumors from 373 women with endometrial cancer using different technologies to look for defects in DNA, RNA (a close chemical cousin of DNA) and proteins.
Their analysis indicates that about 25 percent of women with endometrial cancer who are thought to have a favorable prognosis based on pathology reports instead have a more formidable form of the disease, based on underlying genetic changes, and should be treated aggressively.
Clinically, endometrial cancers fall into two categories: endometrioid and serous. Endometrioid cancers generally are associated with excess estrogen, obesity and a favorable prognosis. In contrast, serous endometrial cancers are more common in older women and generally have poorer outcomes.
After surgery to remove endometrial cancer, women with the endometrioid subtype typically are treated with radiation therapy to kill remaining cancer cells, while those with serous tumors receive a more aggressive treatment chemotherapy.
Doctors distinguish between the two tumor subtypes by evaluating cancer cells under a microscope. But categorizing some tumors is difficult, and pathologists don't always agree.
Looking closely at endometrioid tumors classified as high-grade, meaning they are more likely to grow quickly and spread, the investigators showed that many share genetic features with serous tumors. These include frequent mutations in TP53, a tumor suppressor gene, as well as extensive copy number alterations, which refer to a cell having too many or too few copies of a gene.
"This highlights the benefit of digging deeper to find the genetic drivers of cancer growth," Mardis says. "Even though high-grade endometrioid and serous endometrial cancer are different from a pathological standpoint, they are genetically very similar and may require a similar course of treatment."
With a complete analysis of the tumor samples, the investigators identified four novel genomic-based subtypes of endometrial cancer, which set the stage for developing new ways to diagnose and treat the disease. The subtypes are based, in part, on the frequency of mutations in the tumors.
"The Cancer Genome Atlas' multidimensional approach to collecting genomic data, including clinical and pathology information, have made these findings possible," says Harold Varmus, MD, director on the National Cancer Institute. "Without the integrated characterization of so many tumor samples, correlations between histology and genomic data may not have been observed or potential clinical outcomes identified."
Interestingly, one subtype features an exceedingly high mutation rate in the POLE gene and, in this respect, is similar to an "ultramutated" subtype of colorectal cancer. But, surprisingly, patients with these kinds of tumors generally have good outcomes.
"Having many, many mutations sounds like a bad thing," Mardis explains. "But these patients can't fix the mistakes in their tumor DNA, so their cancer cells mutate themselves into oblivion before they have the opportunity to spread to other locations in the body. The good news for these patients is that their outcomes are excellent, and they don't need aggressive treatment."
Women with serous tumors frequently had mutations in one of two genes that potentially could be targeted with existing targeted therapies. Those with ERBB2 alterations, for example, may be effectively treated with Herceptin, a drug typically used in women with breast cancer who have the same mutation. Additionally, women whose endometrial tumors have PIK3CA mutations may benefit from drugs that inhibit the gene. Those drugs are now in phase II clinical trials.
According to the authors, the new findings provide a roadmap for future clinical trials for endometrial cancer.
"Each tumor subtype may warrant separate clinical trials because of marked genomic differences, which are indicative of different drivers of endometrial cancer," Mardis says. "Developing therapies for each subtype may improve outcomes for many women with endometrial cancer and parallel what has been accomplished in breast cancer."
Endometrial cancer is the fourth most commonly diagnosed cancer among U.S. women. About 50,000 cases will be diagnosed in 2013, and an estimated 8,000 women will die from the disease. For a majority of patients diagnosed with aggressive, high-grade tumors that have spread, the five-year survival rate is about 16 percent, though chemotherapy has been associated with improved survival, and new targeted agents are being tested.
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Levine DA, Mardis ER and The Cancer Genome Atlas Research Network. Integrated genomic characterization of endometrial carcinoma. Nature. May 2, 2013.
The research is funded by the National Institutes of Health (NIH) as part of The Cancer Genome Atlas Project. Grant numbers: 5U24CA143799-04, 5U24CA143835-04, 5U24CA143840-04, 5U24CA143843-04, 5U24CA143845-04, 5U24CA143848-04, 5U24CA143858-04, 5U24CA143866-04, 5U24CA143867-04, 5U24CA143882-04, 5U24CA143883-04, 5U24CA144025-04, U54HG003067-11, U54HG003079-10 and U54HG003273-10.
Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
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Source: http://www.eurekalert.org/pub_releases/2013-05/wuso-gtr042913.php
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LOS ANGELES -- Jillian Michaels didn't think she had another weight-loss book in her. She'd already written several, including "Master Your Metabolism," "Winning by Losing" and "Making the Cut." What else was there to say?
Plenty, as it turns out. Her latest book is "Slim for Life," and it represents Michaels' most accessible approach to health and fitness. Not exactly what you might expect from the star of NBC's "The Biggest Loser," known for ripped abs and a no-excuses, take-no-prisoners approach to diet and exercise.
You see, Superwoman has been transformed into Everywoman.
Michaels' life changed dramatically last May when she became a mother to two: Lukensia, 3, whose adoption from Haiti was finalized the same week that Michaels' partner, Heidi Rhoades, gave birth to their son, Phoenix. Cue the missed workouts, less-than-ideal snacks and - surprise, surprise - not enough sleep.
And 5 extra pounds on the scale.
Now that might not seem like much to us mere mortals, but it gave Michaels a glimpse into the lives of millions of Americans struggling to wedge healthful food choices and exercise into lives packed with work and family obligations.
"It used to be that I didn't accept 'limitations,' " Michaels said over breakfast one recent morning while dining on a bowl of fresh berries at Le Pain Quotidien on Ventura Boulevard, where she was virtually unrecognizable - no makeup, ball cap, sweats and flip-flops - to the diners around her.
"I was like, 'It's a state of mind! No excuses!'
"But adding kids to the mix added a whole 'nother layer of responsibility, of time management, of financial obligations, of no sleep. It definitely made me understand."
It was a point driven home on one day in particular when she looked at her schedule and realized that she had only three hours to spare once she carved out time for work, travel and sleep. "I was sitting there thinking, 'Am I going to work out or do I spend the time with my kids?'"
That's the vantage point of "Slim for Life."
Michaels said she tried to tackle every "excuse" she's heard over the years, including such well-worn favorites as not enough time, not enough money and no idea where to start. "Slim for Life" readers will find hundreds of strategies and tactics for weaving fitness and healthful food choices into their current lives (instead of the other way around.)
"Slim for Life" is intended to be a lifestyle approach, Michaels said, and one that readers will ideally return to again and again as their commitment to health and fitness grows.
Readers are asked to pick from among Michaels' suggestions, but with those choices come consequences. They can take the easy route, but it doesn't come with the eye-popping results that most of us want. The middle road is a bit tougher, and then there's the all-in approach.
Example: When traveling, you can get in lots of walking while sightseeing (easy) or you can find daily calorie-blasting activities that are fun for the family, like paddle boarding (the middle-of-the-road approach). Or you can bring your own fitness DVD collection and laptop and turn your hotel room into your gym (the gung-ho approach).
But what about the real stumbling block for most people, the foods that we love? (Looking at you, chocolate!)
Michaels offers ways to enjoy such favorites while adhering to the 80/20 rule. Anyone who has ever picked up a diet book has heard of this - eat "clean" 80 percent of the time and loosen the reins a bit for 20 percent. But "Slim for Life" has concrete examples of what that actually looks like.
For Michaels, it's taking her daily calories (1,800) and calculating that she can spend 1,450 of those calories on "super-healthy stuff" like fish and leafy greens, leaving her with 350 calories for cookies or ice cream. Or, if a splurge meal is involved, she makes sure to follow that meal with at least five healthful meals, including snacks. "Deprivation is miserable and isn't sustainable. You're not going to go the rest of your life without a bite of chocolate or a piece of pizza." She does not condone a "cheat day" strategy, however, because it's too easy for people to overeat and "wipe out all the hard work they put in during the week."
Another trouble area for many people is food on the job, particularly in big offices where candy dishes, group lunches, happy hour celebrations and birthday cakes are the norm.
Michaels suggests some common sense tactics such as keeping a stash of healthful foods in your desk and takeout menus offering smart food choices within reach. But her strategy for dealing with the never-ending birthday cake extravaganzas is simple and brilliant, and too good not to pass along: "Send a happy birthday email. Explain that you won't be making it over for the celebration because you're 'saving the extra calories' and can't handle the temptation."
"I know that you can't do everything," Michaels said. "But this book is about a lifestyle. This is how I want you to live. ... I'm saying, 'I get it, I feel you, I hear all your obstacles.' I'm going to make it as easy as possible. And it's not going to get easier than this."
Source: http://www.modbee.com/2013/02/15/2579740/is-jillian-michaels-growing-soft.html
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